bs-0047R-FITC [Conjugated Primary Antibody]
Insulin Receptor alpha Antibody, FITC Conjugated
www.biossusa.com
[email protected]
800.501.7654 [DOMESTIC]
+1.781.569.5821 [INTERNATIONAL]
DATASHEET

Host: Rabbit

Target Protein: Insulin Receptor alpha

Immunogen Range: 701-760/1382


Clonality: Polyclonal

Isotype: IgG

Entrez Gene: 3643

Swiss Prot: P06213

Source: KLH conjugated synthetic peptide derived from human Insulin Receptor alpha

Purification: Purified by Protein A.

Storage Buffer: Aqueous buffered solution containing 0.01M TBS (pH 7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.

Storage: Store at -20°C. Aliquot into multiple vials to avoid repeated freeze-thaw cycles.

Background:

Receptor tyrosine kinase which mediates the pleiotropic actions of insulin. Binding of insulin leads to phosphorylation of several intracellular substrates, including, insulin receptor substrates (IRS1, 2, 3, 4), SHC, GAB1, CBL and other signaling intermediates. Each of these phosphorylated proteins serve as docking proteins for other signaling proteins that contain Src-homology-2 domains (SH2 domain) that specifically recognize different phosphotyrosines residues, including the p85 regulatory subunit of PI3K and SHP2. Phosphorylation of IRSs proteins lead to the activation of two main signaling pathways: the PI3K-AKT/PKB pathway, which is responsible for most of the metabolic actions of insulin, and the Ras-MAPK pathway, which regulates expression of some genes and cooperates with the PI3K pathway to control cell growth and differentiation. Binding of the SH2 domains of PI3K to phosphotyrosines on IRS1 leads to the activation of PI3K and the generation of phosphatidylinositol-(3, 4, 5)-triphosphate (PIP3), a lipid second messenger, which activates several PIP3-dependent serine/threonine kinases, such as PDPK1 and subsequently AKT/PKB. The net effect of this pathway is to produce a translocation of the glucose transporter SLC2A4/GLUT4 from cytoplasmic vesicles to the cell membrane to facilitate glucose transport. Moreover, upon insulin stimulation, activated AKT/PKB is responsible for: anti-apoptotic effect of insulin by inducing phosphorylation of BAD; regulates the expression of gluconeogenic and lipogenic enzymes by controlling the activity of the winged helix or forkhead (FOX) class of transcription factors. Another pathway regulated by PI3K-AKT/PKB activation is mTORC1 signaling pathway which regulates cell growth and metabolism and integrates signals from insulin. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 thereby activating mTORC1 pathway.

Conjugation: FITC

Excitation/ Emission: 494nm/518nm

Size: 100ul

Concentration: 1ug/ul

Applications: WB(1:300-5000)
FCM(1:20-100)
IF(IHC-P)(1:50-200)
IF(IHC-F)(1:50-200)
IF(ICC)(1:50-200)

Predicted Molecular Weight: 80/152


Cross Reactive Species: Human
Rat

Predicted Cross Reactive Species: Mouse
Dog
Cow
Sheep
Pig
Horse
Chicken
Rabbit

For research use only. Not intended for diagnostic or therapeutic use.

PRODUCT SPECIFIC PUBLICATIONS
  • Xiao et al. APT070 (mirococept), a membrane-localizing C3 convertase inhibitor, attenuates early human islet allograft damage in vitro and in vivo in a humanized mouse model. (2016) Br.J.Pharmaco. 173:575-87Read more>>
  • Lin IC et al. High fructose diet induces early mortality via autophagy factors accumulation in the rostralventrolateral medulla as ameliorated by pioglitazone. J Nutr Biochem. 2019 Apr 8;69:87-97.Read more>>
VALIDATION IMAGES